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Relaxin and Prostaglandin E₂ Regulate Interleukin 11 during Human Endometrial Stromal Cell Decidualization

Prince Henry’s Institute of Medical Research (E.D., C.S., L.A.S.), Clayton, Victoria 3168, Australia; and The Walter and Eliza Hall Institute of Medical Research (M.B., W.D.F., J.E.M.), Parkville, Victoria 3053, Australia

Address all correspondence and requests for reprints to: Dr. Eva Dimitriadis, Prince Henry’s Institute of Medical Research, P.O. Box 5152, Clayton, VIC 3168, Australia. E-mail: evdokia.dimitriadis{at}phimr.monash.edu.au.

Decidualization of endometrial stromal cells and IL-11 signaling are essential for embryo implantation in the mouse. We investigated the effects of relaxin (RLX) and prostaglandin E₂ (PGE₂) on IL-11 secretion by human endometrial stromal cells (HESC) and during cAMP or medroxyprogesterone acetate (P)-induced decidualization. cAMP-decidualized HESC secreted high levels of IL-11. RLX, cAMP, or PGE₂ increased IL-11 mRNA and IL-11 secretion, with maximal response to RLX and cAMP. Addition of the cAMP/protein kinase A inhibitor Rp-adenosine-3,5-cyclic-monophosphorothioate to either RLX- or PGE₂-treated cells decreased IL-11 secretion. Indomethacin treatment decreased IL-11 secretion, which was largely restored by cotreatment with PGE₂ or RLX. Cotreatment of HESC with RLX, PGE₂, or cAMP and estrogen plus P down-regulated IL-11 mRNA and IL-11 secretion at 24 h, before secretion of prolactin (decidualization marker). Addition of W147AIL-11 (IL-11 signaling inhibitor) reduced prolactin secretion stimulated by RLX or PGE₂ and estrogen plus P. This is the first demonstration that cAMP-decidualized HESC secrete IL-11 and that IL-11 mRNA and IL-11 secretion are regulated by RLX and PGE₂, partly via a cAMP/protein kinase A-dependent pathway. Blocking IL-11 signaling reduced RLX+P- or PGE₂+P-induced decidualization, suggesting that RLX and PGE₂ act via IL-11. This is important in understanding implantation and regulation of fertility.

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